Identification of copper/zinc superoxide dismutase as a nitric oxide-regulated gene in human (HaCaT) keratinocytes: implications for keratinocyte proliferation

Frank, Stefan; Kämpfer, Heiko; Kaufmann, Roland; Pfeilschifter, Josef

doi:10.1042/0264-6021:3460719

Cited by 43 publications

(27 citation statements)

References 48 publications

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“…Moreover, we have been able to functionally connect the enzymatic actions of the Cu,Zn-SOD to keratinocyte proliferation. Nevertheless, overexpression of the SOD enzyme did not alter gene expression in the cells (26). Thus, NO actions on keratinocyte gene expression and proliferation appeared to be clearly dissected in molecular terms, as we had not yet identified a regulatory player in NO-controlled gene expression that also participated in the control of keratinocyte proliferation.…”

Section: Identification Of P68 As a Novel No-regulated Gene In Kera-mentioning

confidence: 95%

“…p68 RNA Helicase and Keratinocytes 44879 low concentrations of NO (26,36). However, it is not particularly known how NO exerts its unique actions on keratinocytes.…”

Section: Identification Of P68 As a Novel No-regulated Gene In Kera-mentioning

confidence: 99%

“…4), although p68 protein levels declined earlier when compared with growth factor-stimulated cells. It is known for some time that a mixture of cytokines also induces iNOS expression in keratinocytes (25,26). To determine a possible role of endogenously produced NO in p68 expression, we treated cells with the cytokines (IL-1␤, TNF-␣, and IFN-␥) in the presence or absence of the nitric-oxide synthase inhibitor N Gmonomethyl-L-arginine.…”

Section: Identification Of P68 As a Novel No-regulated Gene In Kera-mentioning

confidence: 99%

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p68 DEAD Box RNA Helicase Expression in Keratinocytes

Kahlina

Goren

Pfeilschifter

et al. 2004

Journal of Biological Chemistry

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Section: Identification Of P68 As a Novel No-regulated Gene In Kera-mentioning

confidence: 95%

“…p68 RNA Helicase and Keratinocytes 44879 low concentrations of NO (26,36). However, it is not particularly known how NO exerts its unique actions on keratinocytes.…”

Section: Identification Of P68 As a Novel No-regulated Gene In Kera-mentioning

confidence: 99%

Section: Identification Of P68 As a Novel No-regulated Gene In Kera-mentioning

confidence: 99%

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p68 DEAD Box RNA Helicase Expression in Keratinocytes

Kahlina

Goren

Pfeilschifter

et al. 2004

Journal of Biological Chemistry

Self Cite

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“…Among the known antioxidative protein, SOD (superoxide dismutase) is thought to play a central role because of its ability to scavenge superoxide anions, the primary ROS (reactive oxygen species) generated from molecular oxygen in cells [1]. Constitutive SOD1 expression is a normal occurrence in most tissues, except for keratinocytes and glomerular mesangial cells in which nitrosoglutathione induces SOD1 expression [2,3], while SOD2 expression is regulated by a variety of agents, including inflammatory cytokines, lipopolysaccharide and oxidative stress [4,5]. The SOD1 protein is localized in the cytosol and the intermembrane space of mitochondria, whereas the SOD2 protein is exclusively located in mitochondria [6,7].…”

Section: Introductionmentioning

confidence: 99%

Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production

Iuchi

Okada

Onuma

et al. 2007

Biochemical Journal

150

105

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Reactive oxygen species are involved in the aging process and diseases. Despite the important role of Cu/Zn SOD (superoxide dismutase) encoded by SOD1, SOD1 −/− mice appear to grow normally under conventional breeding conditions. In the present paper we report on a novel finding showing a distinct connection between oxidative stress in erythrocytes and the production of autoantibodies against erythrocytes in SOD1 −/− mice. Evidence is presented to show that SOD1 is primarily required for maintaining erythrocyte lifespan by suppressing oxidative stress. A SOD1 deficiency led to an increased erythrocyte vulnerability by the oxidative modification of proteins and lipids, resulting in anaemia and compensatory activation of erythropoiesis. The continuous destruction of oxidized erythrocytes appears to induce the formation of autoantibodies against certain erythrocyte components, e.g. carbonic anhydrase II, and the immune complex is deposited in the glomeruli. The administration of an antioxidant, N-acetylcysteine, suppressed erythrocyte oxidation, ameliorated the anaemia, and inhibited the production of autoantibodies. These data imply that a high level of oxidative stress in erythrocytes increases the production of autoantibodies, possibly leading to an autoimmune response, and that the intake of antioxidants would prevent certain autoimmune responses by maintaining an appropriate redox balance in erythrocytes.

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“…In this context, targeted S-nitrosylation of Panx3 in these cells may serve as an important regulatory element promoting cell growth and differentiation. Nitric oxide also promotes both the proliferation, at low concentrations, and differentiation, at high concentrations, of keratinocytes [292,293]. In these cells, Panx1 and Panx3 act to suppress proliferation and augment differentiation [167,294].…”

Section: Introduction/resultsmentioning

confidence: 99%

Function and Regulation of Pannexin 1 Channels in the Vascular Endothelium

Lohman¹

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The nucleotide adenosine 5'-triphosphate (ATP) has classically been considered the cell's primary energy currency; however, a novel role for ATP as an extracellular autocrine/paracrine signaling molecule has evolved over the past century. Purinergic signaling is now known to regulate a plethora of physiological and pathophysiological processes in almost every organ system. In the vasculature, ATP and its metabolites elicit dual control over blood vessel tone and tissue perfusion, and purinergic signaling events have been implicated in vascular pathologies including atherosclerosis and inflammation.While the importance of extracellular ATP in the vascular system is well recognized, the mechanism(s) mediating the regulated release of the purine from vascular cells are less well understood and are a key target of current investigation. One such ATP-liberation mechanism has been ascribed to the recently identified pannexin (Panx) channels, namely Panx1. Initially, we characterized the expression and localization profiles of Panx isoforms across the systemic vasculature, identifying predominant representation by the Panx1 isoform in both smooth muscle (SMC) and endothelial cells (EC) comprising the blood vessel wall, with more heterogeneous expression profiles observed in specialized vascular systems including the heart, lung and kidney. In particular, the Panx1 isoform is highly expressed in ECs regardless of blood vessel type or size, while Panx1 expression is limited to SMCs of small arteries and arterioles. Panx1 forms hexameric channels in the plasma membrane of ECs, functioning to release ATP in response to a number of stimuli. However, prolonged Panx1 channel activity is extremely detrimental to cell viability. Here we report a novel negative regulatory mechanism that may govern the activity of Panx1 channels in ECs, by which the bioactive gas nitric oxide (NO) covalently modifies two cysteine (Cys) residues in the channel by a process termed S- reinforce the dual effect of purines on peripheral resistance and blood pressure. Purinergic Control of Vascular InflammationWhile the foundation for purinergic control of vascular functions was initially characterized extensively in the context of vascular reactivity and overall blood flow and pressure regulation, it has become increasingly clear that extracellular ATP also plays important regulatory roles in the vascular inflammatory response. Vascular inflammation can be characterized as acute (physiological) or chronic (pathological) in nature.The acute vascular inflammatory response is an innate process of inflammatory cell homing to infected or damaged tissues resulting from integrated cross-talk between circulating leukocytes and the vascular endothelium, primarily at the level of postcapillary venules [61]. This process has been highly studied and is now known to occur in a step-wise manner beginning with local recruitment, rolling (fast and slow), adhesion and final extravasation into the surrounding tissue (reviewed in [62...

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Identification of copper/zinc superoxide dismutase as a nitric oxide-regulated gene in human (HaCaT) keratinocytes: implications for keratinocyte proliferation

Cited by 43 publications

References 48 publications

p68 DEAD Box RNA Helicase Expression in Keratinocytes

p68 DEAD Box RNA Helicase Expression in Keratinocytes

Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production

Function and Regulation of Pannexin 1 Channels in the Vascular Endothelium

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